ArticleCNS neuroscience & therapeutics2025
Myricetin Suppresses Inflammatory Th17 Polarization to Mitigate Alzheimer's Disease Pathogenesis.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Cynanchum bungei Decne-derived extracellular vesicles alleviate cognitive impairment and pathological damage in Alzheimer's disease.Frontiers in cellular neuroscience · 2026Article
- Myricetin Suppresses Inflammatory Th17 Polarization to Mitigate Alzheimer's Disease Pathogenesis.CNS neuroscience & therapeutics · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
aimsThis study aimed to investigate the therapeutic potential of myricetin, a natural flavonoid, in Alzheimer's disease (AD) by targeting Th17 cell-mediated neuroinflammation through inhibition of the transcription factor RORγt.
methodsVirtual screening of 47,963 compounds identified myricetin as a potential RORγt inhibitor, validated by molecular docking and dynamics simulations. In vivo, 3xTg-AD mice were treated with myricetin (50 mg/kg/day) for 8.5 weeks, followed by behavioral tests (novel object recognition, Morris water maze) and pathological analyses (HE/Nissl staining, immunohistochemistry, Western blot). In vitro, Th17 polarization assays and mechanistic studies (ChIP, EMSA, MST) were performed to elucidate myricetin's action on RORγt-IL-17 signaling.
resultsMyricetin exhibited stable binding to RORγt (Kd = 6.40 μM), suppressing Th17 polarization and IL-17 production. In AD mice, myricetin improved cognitive function, reduced neuronal damage, decreased Aβ plaques and phosphorylated tau levels, and attenuated microglial activation. Mechanistically, myricetin blocked RORγt recruitment to the IL17 promoter, downregulating IL-17 transcription.
conclusionMyricetin ameliorates AD pathology by inhibiting RORγt-driven Th17 polarization, highlighting its potential as a therapeutic agent for AD.
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Registered trials
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